DESCRIPTION (adapted from the applicant's description): Abscisic acid is a central stress hormone in plants which mediates rapid cellular responses and down regulates cell proliferation, causes cell cycle arrest and inhibits growth. Early signal transduction mechanisms that down regulate cell proliferation are of central importance for controlling mitogenesis. The long-term goal of this research is to achieve a detailed quantitative understanding of the network of events that mediate early abscisic acid signal transduction in the easily manipulated genetic model system, Arabidopsis thaliana. Abscisic acid (ABA) signal transduction will be analyzed in Arabidopsis guard cells, which provide a powerful system for quantitatively dissecting the complex molecular machinery mediating specificity in early signaling cascades. The hypothesis that the ABI1 and ABI2 phosphatases and ERA1 negatively regulate ABA signaling at different points in the early ABA signaling network will be tested. Using a combination of quantitative cell biological and molecular genetic the specific aims if this proposal include: (1) Determine whether era1F'Tase deletion enhances ABA-induced early cytosolic Ca2+ ([Ca2+]cyt) increases. (2) Determine whether the abi1and abi2 mutants impair Ca2+ entry via the plasma membrane and/or second messenger regulated Ca2+ release from intracellular stores. (3) Determine the cellular locations of the wild-type and mutant ABI protein phosphatases in wildtype and in era1 FTase deletion backgrounds. (4) Identify genes encoding farnesylated targets of ERAl in guard cells. (5) Clone and characterize the function of a new recessive ABA hypersensitive mutant gene, abh1.